Eating Disorders

What is eating disorders?

The eating disorders are classified to three main groups of anorexia nervosa, bulimia and binge-eating disorders. These conditions are serious disturbances in eating behavior and body image. Individuals with eating disorders are often concerned about weight, body shape and body image.


Dfinition Schizophrenia is a chronic and severe mental disorder that affects how a person thinks, feels, and behaves. People with schizophrenia may seem like they have lost touch with reality....

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Opioid abuse

Dfinition Opioids are a group of substances that work on opioid receptors of nervous system. Opioids can be classified to three groups of: Natural: Opium Synthetic: Oxycodone Hydrocodone Methadone Fentanyl...

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Alcohol dependence

Epidemiology of drinking

In 2012, 51.3% of adults 18 years of age and over in the United States were current regular drinkers (at least 12 drinks in the past year) and 12.9% were current infrequent drinkers (1-11 drinks in the past year): 12.9%

There are approximately 88,000 deaths attributable to excessive alcohol use each year in the United States. Excessive alcohol use is the 3rd leading lifestyle-related cause of death for the Americans; responsible for 2.5 million years of potential life lost (YPLL) annually, or an average of about 30 years of potential life lost for each death. The economic costs of excessive alcohol consumption in 2006 were estimated at $223.5 billion.

It is estimated that only 10% to 20% of patients undergoing alcohol withdrawal are treated as inpatients, so it is possible that as many as 2 million Americans may experience symptoms of alcohol withdrawal conditions each year.

Categories of alcohol use:

  1. No use
  2. Low risk use
  3. Hazardous drinking
  4. Alcohol abuse
  5. Alcohol dependence

Health risks related to drinking

Short-Term Health Risks

Excessive alcohol use has immediate effects that are most often the result of binge drinking and include the following:

  • Injuries: (Smith 1999)
    • Traffic injuries
    • Falls
    • Drowning
    • Burns
    • Unintentional firearm injuries
  • Violence:
    • Intimate partner violence and
    • Child maltreatment.
    • About 35% of victims report that offenders are under the influence of alcohol. (Greenfield 1998)
    • Alcohol use is also associated with 2 out of 3 incidents of intimate partner violence. (Greenfield 1998)
    • Studies have also shown that alcohol is a leading factor in child maltreatment and neglect cases, and is the most frequent substance abused among these parents.
  • Risky sexual behaviors
    • Unprotected sex,
    • Sex with multiple partners
    • Increased risk of sexual assault
    • These behaviors can result in unintended pregnancy or sexually transmitted diseases (Naimi et al 2003; Wechsler et al 1994)
  • Miscarriage and stillbirth among pregnant women, and a combination of physical and mental birth defects among children that last throughout life. (Kesmodel 2002)
  • Alcohol poisoning, a medical emergency that can cause loss of consciousness, low blood pressure and body temperature, coma, respiratory depression, or death. (Sanap 2003)

Long-Term Health Risks

  • Long-term excessive alcohol use can lead to the development of chronic diseases, neurological impairments and social problems such as:
    • Neurological
      • Dementia
      • Stroke
      • Neuropathy
    • Cardiovascular problems
      • Myocardial infarction
      • Cardiomyopathy
      • Atrial fibrillation
      • Hypertension
    • Psychiatric problems
      • Depression
      • Anxiety
      • Suicide
    • Social problems
      • Unemployment
      • Lost productivity
      • Family problems
    • Cancers of:
      • Mouth, throat, esophagus, pancreas, stomach, liver, colon, and breast
    • Liver diseases, including:
      • Alcoholic hepatitis.
      • Cirrhosis, which is among the 15 leading causes of all deaths in the United States (Heron 2007)

Alcohol receptors

  • The brain maintains neurochemical balance through inhibitory and excitatory neurotransmitters.
  • The main inhibitory neurotransmitter is γ-amino-butyric acid (GABA), which acts through the GABA-alpha (GABA-A) neuroreceptor.
  • One of the major excitatory neurotransmitters is glutamate, which acts through the N-methyl-D-aspartate (NMDA) neuroreceptor.
  • Alcohol enhances the effect of GABA on GABA-A neuroreceptors, resulting in decreased overall brain excitability.
  • Chronic exposure to alcohol results in a compensatory decrease of GABA-A neuroreceptor response to GABA, evidenced by increasing tolerance of the effects of alcohol.
  • Alcohol inhibits NMDA neuroreceptors, and chronic alcohol exposure results in up-regulation of these receptors. Abrupt cessation of alcohol exposure results in brain hyperexcitability, because receptors previously inhibited by alcohol are no longer inhibited. Brain hyperexcitability manifests clinically as anxiety, irritability, agitation, and tremors. Severe manifestations include alcohol withdrawal seizures and delirium tremens.
  • Kindling:
    • An important concept in both alcohol craving and alcohol withdrawal is the “kindling” phenomenon;
    • the term refers to long-term changes that occur in neurons after repeated detoxifications.
    • Recurrent detoxifications are postulated to increase obsessive thoughts or alcohol craving.5
    • Kindling explains the observation that subsequent episodes of alcohol withdrawal tend to progressively worsen.
    • Although the significance of kindling in alcohol withdrawal is debated, this phenomenon may be important in the selection of medications to treat withdrawal.
    • If certain medications decrease the kindling effect, they may become preferred agents.

Diagnostic Criteria for Alcohol Withdrawal (DSM-IV)

  •  Two (or more) of the following, developing within several hours to a few days after following criterion:
    • Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 beats per minute)
    • Increased hand tremor
    • Insomnia
    • Nausea or vomiting
    • Transient visual, tactile, or auditory hallucination s or illusions
    • Psychomotor agitation
    • Anxiety
    • Grand mal seizures
  • The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning and the symptoms are not due to a general medical condition and are not better accounted for by another mental disorder.

Alcohol withdrawal symptoms

  • Generally, the symptoms of alcohol withdrawal relate proportionately to the amount of alcoholic intake and the duration of a patient’s recent drinking habit.
  • Minor withdrawal symptoms can occur while the patient still has a measurable blood alcohol level. These symptoms may include insomnia, mild anxiety, and tremulousness.
  • Patients with alcoholic hallucinosis experience visual, auditory, or tactile hallucinations but otherwise have a clear sensorium.
  • Seizures: Withdrawal seizures are more common in patients who have a history of multiple episodes of detoxification. Causes other than alcohol withdrawal should be considered if seizures are focal, if there is no definite history of recent abstinence from drinking, if seizures occur more than 48 hours after the patient’s last drink, or if the patient has a history of fever or trauma.
  • Delirium tremens: Alcohol withdrawal delirium, or delirium tremens, is characterized by clouding of consciousness and delirium. Episodes of delirium tremens have a mortality rate of 1% to 5%. (Kasser 2004) Risk factors for developing alcohol withdrawal delirium include concurrent acute medical illness, daily heavy alcohol use, history of delirium tremens or withdrawal seizures, older age, abnormal liver function, and more severe withdrawal symptoms on presentation.
  • Symptoms of Alcohol Withdrawal Syndrome
    • Minor withdrawal symptoms (6 to 12 hours):
      • insomnia,
      • tremulousness,
      • mild anxiety
      • gastrointestinal upset,
      • headache
      • diaphoresis
      • palpitations
      • anorexia
    • Alcoholic hallucinosis (12 to 24 hours):
      • visual, auditory, or tactile hallucinations
      • Symptoms generally resolve within 48 hours.
    • Withdrawal seizures (24 to 48 hours):
      • generalized tonic-clonic seizures
      • Symptoms reported as early as two hours after cessation.
    • Alcohol withdrawal delirium (delirium tremens) (48 to 72 hours):
      • hallucinations (predominately visual),
      • disorientation,
      • tachycardia,
      • hypertension,
      • low-grade fever,
      • agitation,
      • diaphoresis
      • Symptoms peak at five days.

Patient assessment

  1. Quantity of daily alcoholic intake
  2. Duration of alcohol use
  3. Frequency of use
  4. Type of drinks
  5. Time since last drink,
  6. Previous alcohol withdrawals,
  7. Presence of concurrent medical or psychiatric conditions, and
  8. Abuse of other agents
  9. Reason for dinking
  10. CAGE
    1. Cut down
    2. Annoyed
    3. Guilty
    4. Eye-opener
  11. Drink to get high
  12. Drinking alone
  13. Tolerance
  14. Black outs
  15. Intoxications
  16. Seizure
  17. Family history of alcoholism
  18. Medical problems related to drinking:
    1. Liver diseases
    2. Pancreatitis
    3. Esophageal cancer
    4. Cardiomyopathy
    5. Double vision
    6. Gait imbalance
    7. Poor memory
    8. Anemia
    9. Coagulopathy
    10. Wernicke’s-Korsakoff’s encephalopathy

Physical examination

  1. Blood pressure
  2. Pulse rate
  3. Cardiac exam for: Tachycardia, Arrhythmias, congestive heart failure, coronary artery disease
  4. Gastrointestinal bleeding
  5. Signs of liver disease and cirrhosis
  6. Neuropathy
  7. Pancreatitis
  8. CIWA: The revised Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) scale is a validated 10-item assessment tool that can be used to quantify the severity of alcohol withdrawal syndrome, and to monitor and medicate patients going through withdrawal
    1. CIWA-Ar scores of 8 points or fewer correspond to mild withdrawal,
    2. scores of 9 to 15 points correspond to moderate withdrawal, and
    3. Scores of greater than 15 points correspond to severe withdrawal symptoms and an increased risk of delirium tremens and seizures.
  9. In using the CIWA-Ar, the clinical picture should be considered because medical and psychiatric conditions may mimic alcohol withdrawal symptoms.
  10. Certain medications (e.g., beta blockers) may blunt the manifestation of these symptoms.

Laboratory work up

  1. CBC, diff
  2. Liver function test
  3. Urine drug screen
  4. Electrolyte levels
  5. Amylase
  6. Bilirubin, TG, Cholesterol
  7. LDH
  8. PT, PTT, INR
  9. Uric acid
  10. BUN, Creatinine
  11. Ca, Mg
  12. Phosphorus
  13. Protein


  1. Grant  BF, Harford  TC, Dawson  DA, Chou  P, Dufour  M, Pickering  R.  NIAAA’s epidemiologic bulletin no. 35. Prevalence of DSM-IV alcohol abuse and dependence: United States, 1992.  Alcohol Health Res World.  1994;18:243–8.
  2. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed., text revision. Washington, D.C.: American Psychiatric Association, 2000:216.
  3. Kozak  LJ, Hall  MJ, Owings  MF.  National Hospital Discharge Survey: 2000 annual summary with detailed diagnosis and procedure data.  Vital Health Stat 13.  2002;153:1–194.
  4. Malcolm  R, Herron  JE, Anton  RF, Roberts  J, Moore  J.  Recurrent detoxification may elevate alcohol craving as measured by the Obsessive Compulsive Drinking scale.  Alcohol.  2000;20:181–5.
  5. Kasser C, Geller A, Howell E, Wartenberg A. Detoxification: principles and protocols. American Society of Addiction Medicine. Accessed January 20, 2004, at:
  6. Sullivan  JT, Sykora  K, Schneiderman  J, Naranjo  CA, Sellers  EM.  Assessment of alcohol withdrawal: the revised Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA-Ar).  Br J Addict.  1989;84:1353–7.
  7. Reoux  JP, Miller  K.  Routine hospital alcohol detoxification practice compared to symptom triggered management with an Objective Withdrawal Scale (CIWA-Ar).  Am J Addict.  2000;9:135–44.
  8. Wilson  A, Vulcano  B.  A double-blind, placebo-controlled trial of magnesium sulfate in the ethanol withdrawal syndrome.  Alcohol Clin Exp Resp.  1984;8:542–5.
  9. Mayo-Smith  MF.  Pharmacological management of alcohol withdrawal. A meta-analysis and evidence-based practice guideline. American Society of Addiction Medicine Working Group on Pharmacological Management of Alcohol Withdrawal.  JAMA.  1997;278:144–51.
  10. Saitz  R, Mayo-Smith  MF, Roberts  MS, Redmond  HA, Bernard  DR, Calkins  DR.  Individualized treatment for alcohol withdrawal. A randomized double-blind controlled trial.  JAMA.  1994;272:519–23.
  11. Daeppen  JB, Gache  P, Landry  U, Sekera  E, Schweizer  V, Gloor  S, et al.  Symptom-triggered vs fixed-schedule doses of benzodiazepine for alcohol withdrawal: a randomized treatment trial.  Arch Intern Med.  2002;162:1117–21.
  12. Hayashida  M, Alterman  AI, McLellan  AT, O’Brien  CP, Purtill  JJ, Volpicelli  JR, et al.  Comparative effectiveness and costs of inpatient and outpatient detoxification of patients with mild-to-moderate alcohol withdrawal syndrome.  N Engl J Med.  1989;320:358–65.
  13. Hayashida  M, Alterman  A, McLellan  T, Mann  S, Maany  I, O’Brien  C.  Is inpatient medical alcohol detoxification justified: results of a randomized, controlled study.  NIDA Res Monogr.  1988;81:19–25.
  14. Stockwell  T, Bolt  L, Milner  I, Russell  G, Bolderston  H, Pugh  P.  Home detoxification from alcohol: its safety and efficacy in comparison with inpatient care.  Alcohol Alcohol.  1991;26:645–50.
  15. Myrick  H, Anton  RF.  Treatment of alcohol withdrawal.  Alcohol Health Res World.  1998;22:38–43.
  16. Myrick  H, Anton  RF.  Clinical management of alcohol withdrawal.  CNS Spectr.  2000;5:22–32.
  17. Wolf  KM, Shaughnessy  AF, Middleton  DB.  Prolonged delirium tremens requiring massive doses of medication.  J Am Board Fam Pract.  1993;6:502–4.
  18. Malcolm  R, Myrick  H, Roberts  J, Wang  W, Anton  RF, Ballenger  JC.  The effects of carbamazepine and lorazepam on single versus multiple previous alcohol withdrawals in an outpatient randomized trial.  J Gen Intern Med.  2002;17:349–55.
  19. Horwitz  RI, Gottlieb  LD, Kraus  ML.  The efficacy of atenolol in the outpatient management of the alcohol withdrawal syndrome. Results of a randomized clinical trial.  Arch Intern Med.  1989;149:1089–93.
  20. Fleming  MF, Barry  KL, Manwell  LB, Johnson  K, London  R.  Brief physician advice for problem alcohol drinkers. A randomized controlled trial in community-based primary care practices.  JAMA.  1997;277:1039–45.

Attention Deficit Hyperactivity Disorder (ADHD)


  1. 10% of children with ADHD have other learning disabilities
  2. ADHD is one of the most common childhood disorders and can continue through adolescence and into adulthood.
  3. The average age of onset is 7 years old. ADHD affects about 4.1% American adults age 18 years and older in a given year.
  4. The disorder affects 9.0% of American children age 13 to 18 years. Boys are four times at risk than girls. Studies show that the number of children being diagnosed with ADHD is increasing, but it is unclear why.

ADHD subtypes

  • Predominantly hyperactive-impulsive
    • Most symptoms (six or more) are in the hyperactivity-impulsivity categories.
    • Fewer than six symptoms of inattention are present, although inattention may still be present to some degree.
  • Predominantly inattentive
    • The majority of symptoms (six or more) are in the inattention category and fewer than six symptoms of hyperactivity-impulsivity are present, although hyperactivity-impulsivity may still be present to some degree.
    • Children with this subtype are less likely to act out or have difficulties getting along with other children. They may sit quietly, but they are not paying attention to what they are doing. Therefore, the child may be overlooked, and parents and teachers may not notice that he or she has ADHD.
  • Combined hyperactive-impulsive and inattentive
    • Six or more symptoms of inattention and six or more symptoms of hyperactivity-impulsivity are present.
    • Most children have the combined type of ADHD.

Causes of ADHD

Scientists are not sure what causes ADHD, although many studies suggest that genes play a large role. Like many other illnesses, ADHD probably results from a combination of factors. In addition to genetics, researchers are looking at possible environmental factors, and are studying how brain injuries, nutrition, and the social environment might contribute to ADHD.

Genes. Results from several international studies of twins show that ADHD often runs in families. Researchers are looking at several genes that may make people more likely to develop the disorder. Knowing the genes involved may one day help researchers prevent the disorder before symptoms develop. Learning about specific genes could also lead to better treatments.

Children with ADHD who carry a particular version of a certain gene have thinner brain tissue in the areas of the brain associated with attention. This NIMH research showed that the difference was not permanent, however, and as children with this gene grew up, the brain developed to a normal level of thickness. Their ADHD symptoms also improved.

Environmental factors. Studies suggest a potential link between cigarette smoking and alcohol use during pregnancy and ADHD in children. In addition, preschoolers who are exposed to high levels of lead, which can sometimes be found in plumbing fixtures or paint in old buildings, may have a higher risk of developing ADHD.

Brain injuries. Children who have suffered a brain injury may show some behaviors similar to those of ADHD. However, only a small percentage of children with ADHD have suffered a traumatic brain injury.

Sugar. The idea that refined sugar causes ADHD or makes symptoms worse is popular, but more research discounts this theory than supports it. In one study, researchers gave children foods containing either sugar or a sugar substitute every other day. The children who received sugar showed no different behavior or learning capabilities than those who received the sugar substitute. Another study in which children were given higher than average amounts of sugar or sugar substitutes showed similar results.

In another study, children who were considered sugar-sensitive by their mothers were given the sugar substitute aspartame, also known as Nutrasweet. Although all the children got aspartame, half their mothers were told their children were given sugar, and the other half were told their children were given aspartame. The mothers who thought their children had gotten sugar rated them as more hyperactive than the other children and were more critical of their behavior, compared to mothers who thought their children received aspartame.

Food additives. Recent British research indicates a possible link between consumption of certain food additives like artificial colors or preservatives, and an increase in activity. Research is under way to confirm the findings and to learn more about how food additives may affect hyperactivity.

History taking

Inattention and Distractibility symptoms:

  1. Does the child listen to parents and teacher?
  2. Can s/he concentrate?
  3. Is the child easily distracted?
  4. Can he work without supervision?
  5. Is he able to finish the tasks in a timely manner?
  6. Dose he daydreams or looks confused most of the day?

Impulsivity symptoms:

  1. Does the child involve in risk taking behaviors?
  2. Can he wait for his turn?
  3. Does he constantly interrupt others?
  4. Does he react emotionally?

Hyperactivity/Overactivity components:

  1. Speech tone and pressure
  2. Amount of daily physical activity?
  3. Is the kid talkative?

Past medical history:  

  1. Perinatal complications
  2. Developmental delay
  3. Endocrine disorders
  4. Oppositional Defiant Disorder
  5. Tourette’s Syndrome
  6. Sexual abuse history

Growth and development:

  1. Educational history
  2. Abuse
  3. Cruelty toward animals
  4. Involvement in criminal activities
  5. Substance abuse

Family History

  1. ADHD
  2. Conduct disorders
  3. Tick disorders
  4. Developmental disorders
  5. Substance use

Physical examination

  1.  General appearance
  2. Interview with child
  3. Interview with parents and teacher
  4. Thyroid Examination
  5. Neurological exam
  6. Developmental milestones
  7. Hearing impairment

Associated features

  1. Academic failure
  2. Social problems
  3. Emotional instability
  4. School failure
  5. Poor planning, organization and task performance
  6. Speech and language problems
  7. Poor motor coordination
  8. Enuresis
  9. Insatiability

Differential Diagnosis

Conduct disorder

  1. Set fire
  2. Cruel to animals
  3. Lie
  4. Fighting repeatedly
  5. Stealing
  6. boys > girls
  7. hereditary

Oppositional defiant disorder

  1. hostile and defiant behavior against parents, teacher, …
  2. behaves normally around peers
  3. is not cruel to animals
  4. do not lie
  5. is not criminal

Mood disorder

Substance abuse

Antisocial disorder

Diagnostic work up

  1.  TSH
  2. FBS
  3. Blood Lead level



  1. Goal setting for assignments and projects
  2. Educational Interventions for children with ADHD
  3. Educate the family and the school
  4. Counseling for parents and adolescent patients
  5. Family understanding (Coping)


  1. First line (if history of stimulant dependence):
    1. Bupropion (Wellbutrin)
  2. Second line (if history of stimulant dependence):
    1. Long acting stimulants such as (Concerta, Aptensio)
  3. First line (if no history of stimulant abuse):
    1. Methylphenidate LA (Ritalin LA)
    2. Amphetamine-Dextroamphetamine (Adderall XR)
    3. Methylphenidate (Concerta)
    4. Tomoxetine (Strattera) is a Non-stimulant agent (SNRI)
  4. Second line (if no history of stimulant abuse):
    1. SSRI if:
      1. Comorbid Major Depression
      2. Hyper-focused on activity (e.g. computer games)
      3. Obsessive-Compulsive type behavior
      4. Agents
        1. Bupropion (Wellbutrin)
        2. Venlafaxine (Effexor)
    2. TCAs for:
      1. Insomnia
      2. Enuresis
      3. Agents
        1. Imipramine
          1. Start 10 mg PO qhs (Up to 150 mg/day divided bid)
        2. Desipramine (Risk of sudden CV death)
          1. Start 10 mg PO qhs (Up to 150 mg/day divided bid)
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